cervical artery presentation

Cervical Artery DysfunctionCervical Artery Dysfunctionand Manipulation: A Causeand Manipulation: A Cause--

andand--Effect Relationship?Effect Relationship?

Orthopaedic Speaker Series

Royal Jubilee Hospital

Victoria, BC

April 14th, 2009

Dr. Peter Huijbregts, PT, DPT

ObjectivesObjectives

Discuss epidemiology of cervical (vertebrobasilarand internal carotid) artery dysfunction

Discuss anatomy and physiology relevant tocervical arterial dysfunction

Discuss research linking cervical manipulation toartery dysfunction

Discuss relevant clinical (differential) diagnosisDiscuss risk management and emergencyprocedures with regard to cervical arterydysfunction

Note: absence of risk-benefit discussion

Timely?Timely?

Mrs. Sandy Nette, Edmonton, AB

Bilateral vertebral artery dissection

Chiropractic neck manipulation

$ 500-million class-action lawsuit againstchiropractor, his clinic, Alberta College andAssociation of Chiropractors, and AB Ministry ofHealth and Wellness

Benedetti P, McPhail W. Twist and Shout. Globe and Mail, June 14, 2008

Clinical Vignette # 1Clinical Vignette # 1

20-year old female

Fell down stairs and hurt her back

Boyfriend suggested seeing his chiropractor

Over the next months 189 adjustments in 21visits including upper cervical

Note: initial complaint was low back pain…


Rotary neck manipulation resulted ininability to turn head

That night she kept walking into things atwork

Another visit to chiropractor next day


Neck adjustment

Patient immediately began to cry

Left eye rolled up, right roamed randomly

Convulsions


Turned blue, foaming at the mouth, did notrecognize her mother

Coma

Died next day from a traumatic rupture leftvertebral artery

Relevance to Physiotherapy?Relevance to Physiotherapy?

With research evidence supporting its efficacyphysiotherapists routinely use cervicalmanipulation in patients with:

Neck pain

Headache: Cervicogenic, tension-type, migraine

Dizziness: Cervicogenic

19/20 member organizations IFOMT teach uppercervical manipulation

Rivett D, Carlesso L. Safe Manipulative Practice in the Cervical Spine (2008)

Do these patients make up aDo these patients make up abig portion of our daybig portion of our day--toto--dayday

clinical practice?clinical practice?

In other words:In other words:

What is the risk aWhat is the risk aphysiotherapist mightphysiotherapist might

inadvertently cause a strokeinadvertently cause a strokewith cervical manipulation?with cervical manipulation?

Epidemiology Neck PainEpidemiology Neck Pain

• Point prevalence neck pain: 9%

• 6-month prevalence: 54%

• Lifetime prevalence: 66%

• Point prevalence chronic neck pain (>6 months):18%

Douglass AB, Bope ET. Evaluation and treatment of posterior neck pain in familypractice. J Am Board Fam Pract 2004;17:S13-S22.

Guez M, et al. Chronic neck pain of traumatic and non-traumatic origin. ActaOrthop Scand 2003;74:576-579

Epidemiology HeadacheEpidemiology Headache

Cervicogenic headache: 0.4-2.5% in the generalpopulation and up to 15-20% in those with chronicheadaches

Tension-type headache: Two-thirds of males andover 80% of females in developed countries

Migraine headache: 1-year prevalence 6-8% inmales and 15-18% of females in Europe and US

World Health Organization. Headache Fact Sheet. 2008.

Haldeman S, Dagenais S. Cervicogenic headaches: A critical review. Spine J2001;1:31-46

Epidemiology DizzinessEpidemiology Dizziness

Dizziness accounts for 7% of physician visits forpatients over the age of 45

For adults over 65, it is the number one reason tovisit a physician

Approximately 15 to 30% of people experiencingdizziness will seek medical attention

Huijbregts P, Vidal P. Dizziness in orthopaedic physical therapy practice:Classification and pathophysiology. J Manual Manipulative Ther

2004; 12: 196-211


Cervical spine diagnoses were the reason forreferral in 16% of 1,258 outpatient PT patients,second only to lumbar spine-related diagnoses

Headache reported as co-morbidity in 22% of2,433 patients presenting for outpatient PT/OT

Boissonnault WG. Prevalence of comorbid conditions, surgeries, andmedication use in a physical therapy outpatient population: A multi-centered study. J Orthop Sports Phys Ther 1999;29:506-519

Relevance to PhysiotherapyRelevance to Physiotherapy

Now wait a minute…



Why would we as physiotherapists beworried about the association betweenmanipulation and stroke?



Why would we as physiotherapists beworried about the association betweenmanipulation and stroke?

Isn’t this purely a chiropractic problem?


63-year old male

Hypertensive

Right cerebral infarct five years earlier

Four months previously vertebrobasilarinfarct


PHYSIOTHERAPIST applied cervicalmanipulation

Immediate dizziness post-manipulation

Over the next few hours dysarthria,dysphagia, and left-sided paralysis

Medullary infarct


“…The temporal relationship between young healthypatients without osseous or vascular disease whoattend an SMT practitioner and then suffer theserare strokes is so well documented as to be beyondreasonable doubt indicating a possible causalrelationship…”

Terrett AGJ. Vertebrobasilar stroke following spinal manipulation therapy. In:Murphy R. Conservative Management of Cervical Spine Syndromes (2000)


Rare strokes?

Read: Dissection of the vertebral and/orinternal carotid arteries (ICA)

Epidemiology Cervical ArteryEpidemiology Cervical ArteryDissectionDissection

Cervical artery dissection accounts forapproximately 20% of all strokes in young versus2.5% in older patients

Incidence general population: 2.6 per 100,000

Note the low incidence!

Graziano DL, Nitsch W, Huijbregts PA. Positive cervical artery testing in a patientwith chronic whiplash syndrome. J Manual Manipulative Ther 2007;15:E45-E63

Manipulation, Dissection, andManipulation, Dissection, andStroke?Stroke?

Time to review some material?

1. Arterial anatomy

2. Mechanisms of arterial injury

3. Anatomy and physiology of the cervicalarteries

Anatomy: ArteryAnatomy: Artery

Three-layer structureartery

Intima

Media

Adventitia


INTIMA

Layer of endothelial cells lining vessel interior

Rests on basal lamina

Turnover rate 1% per day

Sub-endothelial layer: longitudinally arrangedloose connective tissue and some smooth musclecells

In arteries: Internal elastic lamina, fenestratedelastin allows diffusion to vessel wall


MEDIA

Concentric layers of helically arrangedsmooth muscle cells

Variable amounts of elastic fibers andlamellae, reticular fibers, and proteoglycans

In larger arteries: External elastic laminaseparating media from adventitia


ADVENTITIA

Longitudinally oriented Type I collagen andelastic fibers

Gradually becomes continuous withenveloping connective tissue

Junqueira LC, et al. Basic Histology. 8th ed (1995)

Mechanisms of ArterialMechanisms of ArterialTraumaTrauma

Subintimal hematoma

Intimal tear

Intimal tear with thrombus formation

Intimal tear with embolic formation

Vessel wall dissection with subintimal hematoma

Vessel wall dissection with pseudo-aneurysm

False aneurysm

Subintimal HematomaSubintimal Hematoma

Disruption vasavasorum leads tosubintimal bleedingand occlusion of VAlumen

May also causevasospasm

Intimal TearIntimal Tear

Intima is the least elasticlayer and, therefore, mostlikely to tear

Exposure sub-endotheliallayer causes thrombosis

Clot may propagateproximally or distally

Vasospasm due tothrombin release

Intimal Tear with EmbolizationIntimal Tear with Embolization

Propagating clotextends into lumenand breaks off

Embolus

Distal arterialocclusion andinfarction

Dissection and SubintimalDissection and SubintimalHematomaHematoma

Disruption intima andinternal elastic lamina

Blood dissects these layersfrom muscular media:dissecting aneurysm

Compresses lumen

Exposure sub-endothelialtissue and thrombosis

Dissection and SubintimalDissection and SubintimalHematoma: ReperfusionHematoma: Reperfusion

Hemorrhage mayagain rupture throughintima

Reestablishescommunication withtrue lumen

Recanalization mayoccur

Dissection with PseudoDissection with Pseudo--AneurysmAneurysm

Disruption of media,internal elastic lamina,and intima

Pseudo-aneurysmunder extendingadventitia

May propagate distally

Frequent cause ofocclusion PICA

False AneurysmFalse Aneurysm

Disruption total arterialwall

Peri-arterial hemorrhagecontained in fascia

External compressionlumen

Turbulence in lumen maycause thrombus andembolus formation

Anatomy: Vertebral ArteryAnatomy: Vertebral Artery

V1: ExtraV1: Extra--Vertebral SegmentVertebral Segment

Branches off the subclavian artery and enters thetransverse foramen of C6 in 89% of people

Enters C7 in 3%, C5 in 6%, and C4 in 1% ofpopulation

Anterior boundary formed by anterior scalene andlongus colli muscles

Posterior boundary transverse processes C7-T1and first rib

V2: IntraV2: Intra--Vertebral SegmentVertebral Segment

Runs through transverse foramina C7-C2

Bordered anteromedially by uncovertebraljoints

May be adherent to periosteum of theuncinate processes

Many anatomical variants have beendescribed

V3: AtlantoV3: Atlanto--Axial SegmentAxial Segment

Transverse foramen of C1 is far lateral ascompared to that of C2

This causes a dorsolateral routing of the vertebralartery from the C2 to the C1 transverse foramen

Tethered at C1 and C2 transverse foramina andatlanto-axial membrane

Artery more prone to injury at this segment?

AtlantoAtlanto--Axial Segment andAxial Segment andRotationRotation

V3: AtlantoV3: Atlanto--Axial SegmentAxial Segment

After exiting the C1 transverse foramen the arteryruns medially in a sulcus in the lateral mass of theatlas

Anatomical variant: Arcuate foramen andponticulus posterior in posterior arch atlas

Anterior boundary is formed by the C0-C1 joint

Posterior boundary is formed by the obliquuscapitis superior and rectus capitis posterior majormuscles

V4: Subforaminal and IntraV4: Subforaminal and Intra--CranialCranial SegmentSegment

Pierces the posterior atlanto-occipitalmembrane and dura and arachnoid mater

Courses on intra-cranially in subarachnoidspace

Cervical BranchesCervical Branches

Spinal rami branch off the vertebral arteryand enter the intervertebral foramen wherethey split in anterior and posterior radiculararteries, anterior central artery, and anteriorand posterior vertebral canal arteries

Radicular arteries supply the anterior andposterior nerve roots and spinal ganglion

The other branches supply epidural tissues

Cervical BranchesCervical Branches

Muscular, cutaneous, and articular rami supply thelocal joints, intrinsic cervical muscles, and the skininnervated by the dorsal ramus of the cervicalspinal nerves

These branches also supply the flaval andinterspinal ligaments

The ascending axial arteries supply the body andodontoid process of C2 and the alar, transverse,and cruciform ligaments

SubSub--Foraminal BranchesForaminal Branches

Subforaminal branches include the anterior,posterior, and lateral spinal arteries

The posterior spinal artery also frequentlybranches off from the posterior inferior cerebellarartery

Below C4 these spinal arteries form anastosmoseswith the spinal rami of the vertebral arteriesthrough the anterior radicular arteries

This leaves the upper cervical cord vulnerable tovascular ischaemia: Implication?

IntraIntra--Cranial BranchesCranial Branches

The posterior inferior cerebellar artery (PICA)branches off before coalescence of the vertebralarteries into the basilar artery

PICA supplies the dorsolateral medulla oblongata,the cerebellar vermis, and a number of cerebellarnuclei

The basilar artery supplies the medulla oblongata,the pons, the mesencephalon, and parts of thecerebellum

IntraIntra--Cranial BranchesCranial Branches

The labyrinthine arteries branch off early from thebasilar artery or the anterior inferior cerebellararteries, which makes the vestibular nucleus andthe inner ears very susceptible to ischaemicabnormalities

The posterior cerebral arteries branch off thebasilar artery and supply the thalamus andhypothalamus and the occipital and temporal lobes

Oostendorp R. Functionele Vertebrobasilaire Insufficientie. PhD Thesis.Nijmegen, The Netherlands: Katholieke Universiteit Nijmegen, 1988.

Anatomy: Internal carotidAnatomy: Internal carotidarteryarteryFig 2

C6

C1 (atlas)

Vertebral ArteryInternal Carotid Artery

Anatomy: ICAAnatomy: ICA

Provides 80% of blood flow to the brainversus 20% supplied by the vertebrobasilarsystem

Traverses sternocleidomastoid, longuscapitis, stylohyoid, omohyoid, and digastricmuscles

Anatomy: ICAAnatomy: ICA

Fixed to the anterior aspect of the C1vertebral body and in the carotid canal inthe petrous bone

Sustained rotation and extension-rotationtests have also been proposed as tests ofICA function

Current Emphasis on ICA:Current Emphasis on ICA:Let’s Put This in PerspectiveLet’s Put This in Perspective

Terrett only found five cases (2.7%) of 185reported cervical artery injuries associated

with SMT involving the ICA

Terrett AGJ. Current Concepts: Vertebrobasilar Complications followingSpinal Manipulation (2001)

Serious ManipulationSerious Manipulation--RelatedRelatedAdverse EventsAdverse Events

Two types of vertebral arterystroke:

1. Wallenberg syndrome

2. Locked-in syndrome

Wallenberg SyndromeWallenberg Syndrome

Dorsolateral medullary syndrome ofWallenberg

Occlusion PICA

Other cause: Occlusion parent vertebralartery, a.k.a. syndrome of BabinskiNageotte

Due to destruction nuclei and pathways indorsolateral medulla oblongata


Inferior cerebellar peduncle: ipsilateral ataxia andhypotonia

Descending spinal tract and nucleus CN V: loss ofpain and temperature sensation ipsilateral face andloss corneal reflex

Ascending lateral spinothalamic tract: loss of painand temperature sensation contralateral trunk andlimbs (alternating analgesia)


Descending sympathetic tract: IpsilateralHorner’s syndrome

Lower vestibular nuclei: Nystagmus,vertigo, nausea, and vomiting

Nucleus ambiguous of glossopharyngealand vagus nerves: Hoarseness, dysphagia,or intractable hiccups

LockedLocked--In SyndromeIn Syndrome

Cerebromedullospinal disconnectionsyndrome

Occlusion mid-basilar artery

Bilateral ventral pontine infraction

Effectively transects brain stem at mid-ponsregion

Patients are “conscious, paralyzed mutes”


Consciousness retained because reticularformation midbrain and rostral pons isunaffected

Cerebrospinal tracts destroyed: Decerebraterigidity

Nuclei CN V-XII destroyed: Also affectsoculomotor nerve (CN III) due todescending neuronal connections


Cutaneous sensation may be grossly intactbecause lateral spinothalamic tract locatedlaterally in brain stem is spared

Auditory nerves ascend brainstem lateral toinfarct area: Patient still can hear

CN IV spared: Eye convergence andupward gaze intact

BradfordBradford--Hill Criteria forHill Criteria forCausationCausation

Biologically plausible

Proposed cause temporally related tooccurrence

Consistent across different samples andgroups

Positive correlation exposure andoccurrence

No other explanation

BradfordBradford--Hill Criterion # 1:Hill Criterion # 1:Biological PlausibilityBiological Plausibility

It is certainly biologically plausible thatexcessive mechanical force imparted to the

artery could cause arterial wall damage

Evidence Linking ManipulationEvidence Linking Manipulationto Stroketo Stroke

Terrett (1995): Narrative review of English,French, German, Scandinavian, and Asianliterature 1934-2000: 185 cases reported,death in 30 cases


Updated in 2001: 236 cases reported

Triano and Kawchuk (2006) updated thisreview and found reports of 80 additionalcases of post-manipulation complications

Triano JJ, Kawchuk G. Current Concepts in SpinalManipulation and Cervical Arterial Incidents (2006)


DiFabio (1999): systematic review overperiod 1925-1997

177 cases with mostly arterial dissection orspasm, brain stem lesion, and Wallenbergsyndrome

Death resulted in 18% (n=32)

Also visual defects, hearing loss, balancedeficits, and phrenic nerve damage


Cervical manipulation NOT a new treatment in41% of patients

When described rotational thrust seemed mostinjurious (23%)

However, technique described in only 54%

DiFabio RP. Manipulation of the cervical spine: Risks and benefits. PhysTher 1999;79:50-65


Ernst (2002): Systematic review over 1995-2001period

42 cases with serious adverse events: Mainlyarterial dissection

Also long thoracic nerve palsy, disk herniations,myelopathy, epidural hematoma


Insufficient data on type of manipulation used

Underreporting bias?

Ernst E. Manipulation of the cervical spine: A systematicreview of case reports of serious adverse events, 1995-2001. Med J Aust 2002;176:376-380


True risk remains unknown

Estimated risks adjusted assuming a reporting rateof only 10% in literature

All complications: 5-10 per 10 million

Serious complications: 6 in 10 million

Risk of death: 3 in 10 million

Hurwitz EL, et al. Manipulation and mobilization of the cervical spine: Asystematic review of the literature. Spine 1996;21:1746-1759


582 cases of vertebrobasilar accidents (VBA) inON, 1993-1998

Age and sex-matched controls from provincialinsurance database

Exposure to chiropractic using provincialinsurance data

VBA< 45 years old 5 times more likely (95% CI1.31-43.87) to have visited a chiropractor within 1week before VBA


Also, in younger age group 5 times as likely tohave had ≥ 3 visits with cervical diagnosis inmonth before VBA (95% CI 1.34-18.57)

No significant associations for those over 45 yearsold

Further prospective study indicated; sources ofbias acknowledged

Rothwell DM, Bondy SJ, Williams JI. Chiropractic manipulation andstroke: A population-based case control study. Stroke 2001;32:1054-

1060

Evidence Linking ManipulationEvidence Linking Manipulationto Stroke?to Stroke?

Population-based study over period 1993-2001

818 subjects with VBA stroke

Case crossover portion: 4 control periodsrandomly chosen from the year before the stroke

Case control portion: 4 age and sex-matchedcontrols from provincial insurance database


Case control study

Visiting chiropractor in month before stroke

> 45: OR 0.83 (95% CI: 0.52-1.32)

< 45: OR 3.13 (95% CI: 1.48-6.63)


However,…

Case control study

Visiting GP in month before stroke

> 45: OR 2.67 (95% CI: 2.25-3.17)

< 45: OR 3.57 (95% CI: 2.17-5.86)


“… [A similar association betweenchiropractic and GP visits in the monthbefore the stroke event] suggests that

patients with undiagnosed VA dissectionare seeking clinical care for headache andneck pain before having a VBA stroke…”

Cassidy JD, et al. Risk of vertebrobasilar stroke andchiropractic care. Spine 2008;33:S176-S183.

First Relevant QuestionFirst Relevant Question

How do we identify patients at riskfor cervical artery dysfunction?

Second Relevant QuestionSecond Relevant Question

How do we identify patients with cervicalartery dysfunction in progress?

They are not all this easy…They are not all this easy…

Presenting Complaint?Presenting Complaint?

Major presenting complaint of 137 patientswho subsequently had an SMT-inducedvertebrobasilar vascular incident

Presenting ComplaintPresenting Complaint

47.4%: Neck pain and stiffness

19.7%: Neck pain, stiffness, and headache

16.8%: Torticollis

2.2%: Low back pain

2.2%: Abdominal complaint

1.5%: (Kypho) scoliosis

1.5%: Head cold

1.5%: Upper thoracic pain

0.7%: Upper limb numbness

0.7%: Hay fever

Terrett AGJ. Vertebrobasilar stroke following spinal manipulationtherapy. In: Murphy R. Conservative Management of Cervical SpineSyndromes (2000)

What about Risk Factors?What about Risk Factors?Atherosclerosis

Hypertension

Hypercholesterolaemia

Hyperlipidaemia

Hyperhomocysteinaemia

Diabetes mellitus

Genetic clotting disorders

Infections

Smoking

Free radicals

Upper cervical instability

Migraine

Direct vessel trauma

Autosomal polycystic kidneydisease

Iatrogenic causes

Endothelial inflammatorydisease (e.g., temporalarteriitis)

Arteriopathies

Age

Female gender

Thyroid disease

Oral contraceptive use

Direct Vessel Trauma:Direct Vessel Trauma:

Manipulation

Whiplash

Direct Vessel Trauma:Direct Vessel Trauma:WhiplashWhiplash

In a retrospective analysis, Beaudry andSpence attributed 70 of 80 traumaticallyinduced cases of vertebrobasilar ischaemiato motor-vehicle accidents

Beaudry M, Spence JD. Motor vehicle accidents: The most common causeof traumatic vertebrobasilar ischaemia. Can J Neurol Sci 2003;30:320-

325

Whiplash and DizzinessWhiplash and Dizziness

Dizziness, vertigo, and dysequilibrium aresymptoms in 20-58% of individuals that

have sustained a whiplash-type injury of thecervical spine or a closed head injury

Wrisley DM, et al. Cervicogenic dizziness: A review ofdiagnosis and treatment. J Orthop Sports Phys Ther2000;30:755-766

Whiplash and DizzinessWhiplash and Dizziness Damaged peripheral labyrinth or cochlea in 90% and both

in 69% of 227 post-whiplash patients at neurologyevaluation

92% met the diagnostic criteria for inner ear contusion

Of this subgroup, 63% was diagnosed with BPPV, 64%with secondary endolymphatic hydrops, and 21% withunilateral or bilateral perilymphatic fistulae

25% prevalence of BPPV in 273 consecutive patients withrear-end impact whiplash injury without head injury

Grimm RJ. Inner ear injuries in whiplash. J Whiplash Rel Disord 2002:1:65-75;Oostendorp RAB, et al. Dizziness following whiplash injury: A neuro-otological studyin manual therapy practice and therapeutic implication. J Manual Manipulative Ther1999;7:123-130

Not all Dizziness Implies CADNot all Dizziness Implies CAD

Benign Paroxysmal Positional Vertigo

Cervicogenic dizziness

Vertebrobasilar insufficiency

Dizziness type Nystagmus and dizzinesscharacteristics

Associated signs andsymptoms

Cervicogenicdizziness

Positioning-type No latency period Brief duration Fatigable with

repeated motion

Nystagmus Neck pain Suboccipital

headaches Cervical motion

abnormality onexamination

BPPV Positioning-type Short latency: 1-5seconds

Brief duration: <30seconds

Fatigable withrepeated motion

Nystagmus

Cervicalarterydysfunction

Positional-type Long latency: 55+/-18 seconds

Increasingsymptoms and signswith maintainedhead position

Not fatigable withrepeated motion

Ischaemic and(depending on etiology)possibly non-ischaemicsigns and symptoms asdescribed in Table 10

HallpikeHallpike--Dix ManeuverDix Maneuver

Positional nystagmuson this test has beenshown to identifypatients with posteriorSCC BPPV with 78%sensitivity

Specificity as high as88% has been reported

Age: 30Age: 30--45 year old?45 year old?

Gender: FemaleGender: FemalePredisposition?Predisposition?

Terrett (1995) literature review of 185 patientswith severe CSMT complications

Gender known for 180

77 males (42.8%) of whom 13 died (16.9%)

103 females (57.2%) of whom 17 died (16.5%)

Reflects of male-female ration in chiropracticoffice: 40.7-59.3% or 44.8-55.2%?

ArteriopathiesArteriopathies

Marfan syndrome

Ehlers-Danlos syndrome

Fibromuscular dysplasia

Cystic medial necrosis

Osteogenesis imperfecta

Alpha-1-antitrypsin deficiency

Autosomal dominant polycystic kidney disease

Marfan SyndromeMarfan Syndrome

Higher reported incidence of CAD

Typically show signs of impaired skeletal integrityresulting in joint hypermobility

Extremely arched palate with crowded teeth

Long limbs, spider-like fingers: Arachnodactyly

chest abnormalities: Pectus excavatum

Kyphoscoliosis

Sometimes only vascular defects with minimal orno outward clinical manifestations

EhlersEhlers--Danlos SyndromeDanlos Syndrome

Higher reported incidence of CAD

Vascular Type IV variant may play a role infamilial CAD

History of easy bruising

Thin skin with visible veins

Characteristic facial features: Protruding eyes,small chin, thin nose and lips, and sunken cheeks

Martin JJ, et al. Familial cervical artery dissections: Clinical,

morphologic, and genetic studies. Stroke 2006;37:2924-2929

Hypermobility: Beighton ScoreHypermobility: Beighton Score

Hypermobility: Brighton CriteriaHypermobility: Brighton Criteria

Fibromuscular DysplasiaFibromuscular Dysplasia

Rare non-atherosclerotic and non-inflammatory vascular condition

Primarily affects medium-sized arteries, inparticular the ICA and renal arteries

Present in females 3 to 4 times morefrequently than in males

Bilateral in 65% of patients

Fibromuscular DysplasiaFibromuscular Dysplasia

May be related to mechanical stress to the arterialwall, ischaemia within the vessel due todisturbance of the vasa vasorum, or hormonalactivity that negatively affects the muscular wall

Present in up to 23% of patients with ICAdissection

Presenting complaint may vary from TIA toheadache and dizziness

Cystic Medial NecrosisCystic Medial Necrosis

Focal degeneration of the elastic tissue andmuscle of the tunica media, with thedevelopment of mucoid material

Associated with a variety of systemicdisorders

Typically occurs in patients > 40

Male: female ratio = 2:1

Cystic Medial NecrosisCystic Medial Necrosis

Typically affects large arteries, chiefly theaorta

Sometimes associated with the cervicalarteries

Breakdown of collagen, elastin, and smoothmuscle, along with an increase in theartery’s ground substance

Ehlers-Danlos and Marfan syndrome

Osteogenesis ImperfectaOsteogenesis Imperfecta

Bone fragility

Also blue sclerae, diminished hearing,thinness of the skin, and joint hypermobility

Type 1 associated with CAD: Decreased orstructurally defective type I collagenproduced

AlphaAlpha--11--Antitrypsin DeficiencyAntitrypsin Deficiency

• Circulating serine proteinase inhibitor ofproteolytic enzymes that contributes tomaintenance of integrity of connective tissues

• Deficiency provides insufficient protection againsteffect collagenase and elastase and may damagevessel wall

• Genetic systemic disorder with lung and liverdisease

AlphaAlpha--11--Antitrypsin DeficiencyAntitrypsin Deficiency

• 22 consecutive patients with SCAD and 113 controls with non-CADstroke

• Significantly lower levels in CAD (P=0.01)

• OR 17.7 (95% CI: 2.9-105.6) for A1-AT levels < 90 mg/dl

Findings were refuted by a more recent and methodologically soundstudy

Another small study consisting of 12 spontaneous CAD patients found3 cases with a deficiency of alpha-1-antitrypsin

Overall, there is little evidence in support of this relationship

Vila N, et al. Levels of α1-antitrypsin in plasma and risk of spontaneous cervicalartery dissections. Stroke 2003;34:e168-169; Haneline M, Lewkovich GN. Anarrative review of pathophysiological mechanisms associated with cervical

artery dissection. J Can Chiropr Assoc 2007; 51(3):146–157

Autosomal DominantAutosomal DominantPolycystic Kidney DiseasePolycystic Kidney Disease

Common heritable condition: Prevalence rate of 1in 400 to 1 in 1000

Affecting the renal system

May also lead to extra-renal complications,including connective tissues disorders

Haneline M, Lewkovich GN. A narrative review of pathophysiologicalmechanisms associated with cervical artery dissection. J Can Chiropr

Assoc 2007; 51(3):146–157

Cardiovascular Risk FactorsCardiovascular Risk Factors

Hypertension

Tobacco use

Hypercholesterolaemia

Diabetes

Atherosclerosis

HypertensionHypertension

Frequency of tobacco use, hypertension,diabetes, and hypercholesterolaemia

Group of 153 consecutive patients withCAD, a group of patients with ischaemicstroke unrelated to CAD, and a group ofcontrols

HypertensionHypertension

Hypertension was the only one of 4variables significantly associated withCAD, but only in the subgroup of CADpatients who developed cerebral infarction

Overall OR 1.94 (95% CI: 1.01-3.70)

For VA dissection OR 2.69 (95% CI:1.20-6.04)

AtherosclerosisAtherosclerosis

362 cadaver vertebral arteries

Grade 0 (0% occlusion) to grade 5 (75%occlusion) atherosclerosis

Highest incidence of grade ofatherosclerosis: Grade 3

Mainly in atlanto-occipital portion of VA:4.0%

Also in intra-cranial portion of VA: 35.2%

AtherosclerosisAtherosclerosis

Blood flow proportional to fourth power ofdiameter

Population at risk for developing VBI

Mitchell J. Vertebral artery atherosclerosis: A risk factor in the use of

manipulative therapy? Physiother Res Int 2002;7:122-13

HypercholesterolaemiaHypercholesterolaemia

Prospective study on infection as risk factor forCAD

47 consecutive patients with spontaneous CADand 52 with ischemic stroke

Significantly higher hypercholesterolaemia incontrols (42.6%) versus subjects (12.9%)

Guillon B, et al. Infection and the risk of spontaneous cervical artery

dissection. Stroke 2003;34:e79-e81


72 CAD patients compared with 72 non-CAD stroke control patients

Diabetes, current smoking,hypercholesterolaemia, and oralcontraceptive use not associated with CAD

Pezzini A, et al. History of migraine and the risk of spontaneous cervicalartery dissection. Cephalagia 2005;25:575-580


So: Hypercholesterolaemia is protective?

Hypercholesterolaemia more frequent insubgroup of CAD patients with ischaemicevents

Arnold M, et al. Vertebral artery dissection: Presenting findings andpredictors of outcome. Stroke 2006;37:2499-2503

Thyroid diseaseThyroid disease

Case-control study involving 58 subjects

Present in 31.0% of CAD patients (9/29),compared with 6.9% of non-CAD stroke patients(2/29) (P=0.041)

Immunologic mechanisms contributing to thevascular damage?

Reports of ICA dissection in patients with Gravesdisease: Effects of thyroid hormones on thesmooth muscle cells and endothelium of thevascular system


39-year old male

Felt dizzy and clammy

Consulted osteopath and received tractionmanipulation

Semi-comatose state and vomiting

Died in hospital 19 hours later

Cerebellopontine infarction followingbilateral vertebral artery dissection

InfectionInfection Seasonal variation incidence of CAD: related to

the higher incidence of upper respiratoryinfections during the winter?

31.3% (95% CI: 26.5-36.4) of cohort of 352 CADpatients developed dissection in the winter

Statistically significantly more than in the spring,25.5% (95% CI: 21.1-30.3), the summer 23.5%(95% CI: 19.3-28.3), and the autumn 19.7% (95%CI: 15.7-24.1)

Paciaroni M, et al. Seasonal variability in spontaneous cervical arterydissection. J Neurol Neurosurg Psychiatry 2006;77:677-679

InfectionInfection

• Prospective study on infection as risk factor for CAD

• 47 consecutive patients with spontaneous CAD and 52with ischemic stroke

• Acute infection present within 4 weeks preceding vascularevent more common in SCAD (31.9%) than controlsubjects (13.5%)

• Crude OR 3.0 (95% CI: 1.1-8.2, P= 0.032)

• Adjusted OR 3.1 (95% CI: 1.1-9.2)

Guillon B, et al. Infection and the risk of spontaneous cervical arterydissection. Stroke 2003;34:e79-e81

Oral Contraceptive UseOral Contraceptive Use

One retrospective case-control study(17subjects, 24 controls) investigating CADrisk factors generated statisticallysignificant findings

Current (but not past) use of oralcontraceptives associated with CAD

Oral Contraceptive UseOral Contraceptive Use

Another case-control study that explored CADrisk factors found that 58.3% of CAD cases wereusing oral contraceptives (27 of 47), as comparedwith 40.0% of the controls who had ischemicstroke from another cause (21 of 52): non-significant difference

No consensus

Haneline M, Lewkovich GN. A narrative review of pathophysiologicalmechanisms associated with cervical artery dissection. J Can ChiroprAssoc 2007; 51(3):146–157

Other Risk FactorsOther Risk Factors

Mechanical stress of coughing, sneezing, orvomiting: OR 1.6 (95% CI: 0.67-3.80)

Vascular risk factors OR 0.14 (95% CI: 0.34-0.65)

Current smoking habit OR 0.49 (95% CI: 0.18-1.05)

Triano JJ, Kawchuk G. Current Concepts in Spinal Manipulation andCervical Arterial Incidents (2006)

Systematic Review of RiskSystematic Review of RiskFactors CADFactors CAD

Systematic review risk factors cervicalartery dissection

Two computerized databases, 1966-2005

31 case control studies


Aortic root diameter > 34 (mm): OR=14.2(95% CI: 3.2-63.6)

Homocysteine levels (may causeendothelial damage): OR=1.3 (95% CI:1.05-1.52)


Migraine: OR=3.6 (95% CI: 1.5-8.6)

Trivial trauma (neck manipulation): OR=3.8 (95%CI: 1.3-11)

Recent infection: OR=1.6 (95% CI: 0.67-3.80)

Most studies major sources of bias

Rubinstein SM, et al. A systematic review of the risk factors for cervical

artery dissection. Stroke 2005;36:1575-1580

So Where Does This LeaveSo Where Does This LeaveUs?Us?

Presenting complaint provides no relevantinformation

Clinically relevant risk factors: Previousmedical history of treatment with cervicalmanual therapy interventions, hypertension,previous infection, and migraine headache

Questionable risk factors: Atherosclerosis,thyroid disease, and arteriopathies…

Physical Examination?Physical Examination?

De KleynDe Kleyn--Nieuwenhuyse TestNieuwenhuyse Test

In 1927, De Kleyn and Nieuwenhuysereported decreased or even absent vertebralartery blood flow based on cadaverperfusion studies in different head and neckpositions

De KleynDe Kleyn--Nieuwenhuyse TestNieuwenhuyse Test

Based on these anatomical observations and theseearly perfusion studies, the sustained extension-rotation and the sustained rotation tests have beenproposed and widely instructed and used as teststo determine the presence of vertebrobasilar arterydysfunction

De Kleyn A, Nieuwenhuyse AC. Schwindelanfälle und Nystagmus beieiner bestimmten Stellung des Kopfes. Acta Otolaryngologica1927;11:155-157

Sustained ExtensionSustained Extension--RotationRotationTest and VATest and VA

Extensively studied with equivocal results

Some authors have reported significantdecreases in VA blood flow, whereas otherstudies found no changes

Case reports have noted false negativeresults

Case series have reported 75-100% falsepositive results

Sustained Rotation Test andSustained Rotation Test andVAVA

Research findings for the sustained cervicalrotation test are equally equivocal

Significant decreases or no effect noted onvertebral artery blood flow or volume

Sustained ExtensionSustained Extension--RotationRotationTest and VATest and VA

Meta-analysis of Doppler studies of VA bloodflow velocity

Effect size: Cohen’s d

VA blood flow velocity compromised more inpatients than asymptomatic subjects, oncontralateral rotation, in sitting more than lying,intra-cranial more than cervical

Mitchell J. Vertebral artery blood flow velocity changes with cervical spine rotation: A meta-analysis ofthe evidence with implications for professional practice. J Manual Manipulative Ther 2009;17:46-57.

Sustained (Extension)Sustained (Extension)Rotation Test and ICARotation Test and ICA

Refshauge noted an increase in right ICAblood flow velocity with sustainedcontralateral rotation in healthy volunteers


In contrast, Licht et al found no change in peakflow or time-averaged mean flow velocity in theICA during sustained extension-rotation test

Patients nonetheless experienced symptoms(vertigo, visual blurring, nausea, hemicranialparaesthesiae) classically considered a positiveresponse on this test

Licht PB, Christensen HW, Høilund-Carlsen PF. Carotid artery bloodflow during premanipulative testing. J Manipulative Physiol Ther2002;25:568-572.


Rivett et al reported increase in ICA blood flowvelocity with cervical extension due to narrowingin the ICA?

Decrease in peak systolic and end-diastolic bloodflow velocity in both ICA during sustainedrotation

Found no between-group differences for subjectsthat were positive or negative on this test

Rivett DA, Sharpless KJ, Milburn PD. Effect of premanipulative testson vertebral artery and internal carotid artery blood flow: A pilotstudy. J Manipulative Physiol Ther 1999;22:368-375.

Psychometric DataPsychometric Data

Duplex Doppler ultrasonography

Measured blood flow and vessel diameter

Subjects 1,108 consecutive subjects referred forneurovascular evaluation

136 (12.3%) had unexplained vertebrobasilardistribution symptoms

Extension-rotation position held for at least 10seconds

Sakaguchi M, et al. Mechanical compression of the extracranial vertebral

artery during neck rotation. Neurol 2003;61:845-847


Richter and Reinking calculated diagnosticaccuracy statistics

Comparing signs and symptoms withextension rotation as clinical test and USfindings as reference test

Richter RR, Reinking MF. Evidence in Practice. Phys Ther 2005;85:589-599


Sensitivity 9.3% (95% CI: 4-19.9%)

Specificity 97.8% (95% CI: 96.7-98.5%)

LR+ 4.243 (95% CI: 1.678-10.729)

LR- 0.928 (95% CI: 0.851-1.011)

Interpretation?


12 experimental and 30 control subjects recruitedfrom chiropractic clinics

Experimental group had history of symptomsrelated to head and neck movement and positiveWallenberg test (head and neck extension-rotationfor 30 seconds)

Non-vascular causes excluded by radiography andneurologist examination

Côté P, et al. The validity of the extension-rotation test as a clinicalscreening procedure before neck manipulation: A secondary analysis.J Manipulative Physiol Ther 1996;19:159-164


Extension-rotation test held for 30 seconds

Doppler ultrasound at C3-C5: Systolic peakvelocity to end-diastolic minimum velocity

Positive index test: Vertigo, nausea,tinnitus, lightheadedness, visual problems,numbness of the face or one side of thebody, nystagmus, vomiting, or loss ofconsciousness

Predictive ValidityPredictive Validity

How can positional testing ofhaemodynamics in a still patent vessel beexpected to produce clinically usefulinformation regarding the risk of injury withmanipulative interventions?


With an already pathologically weakened vesselwall, performing the test itself might put thepatient at greater risk due to the potentialstretching forces exerted

At least in cadaver studies, strain values producedduring the test exceeded those produced withmanipulation

Thiel H, Rix G. Is it time to stop functional pre-manipulation testing of the

cervical spine? Man Ther 2005;10:154-158


Haldeman et al did a retrospective analysis of 64medicolegal records describing cerebrovascularischaemia after cervical SMT

The clinicians involved described doing thesustained extension-rotation test in 27 cases

None of these patients had adverse responses

Haldeman S, et al. Unpredictability of cerebrovascular ischaemiaassociated with cervical spine manipulation therapy: A review of sixty-

four cases after cervical spine manipulation. Spine 2002;27:49-55

Again, Where Does ThisAgain, Where Does ThisLeave Us?Leave Us?

Presenting complaint

Clinically relevant risk factors

Questionable risk factors

Sustained extension-rotation test would atthe very most only seem relevant whenpositive

Teaching Provocative TestsTeaching Provocative Tests

17/20 member organizations IFOMT teachprovocative tests involving rotation +/-extension

In March 2004, clinic directors of all USchiropractic colleges agreed to abandonteaching provocative tests

Rivett D, Carlesso L. Safe Manipulative Practice in the Cervical Spine (2008)

Clum G. Cervical Spine Adjusting and the Vertebral Artery (2006)

Remember the Two RelevantRemember the Two RelevantQuestions?Questions?

Goals of history and examination

Screen patients at risk for adverse effectwith intervention

Identify patients with cervical arterydysfunction in progress?

FiveFive DDss AAnd Threend Three NNss

Dizziness

Drop attacks

Diplopia (including amaurosis fugax and cornealreflux)

Dysarthria

Dysphagia (including hoarseness and hiccups)

Ataxia of gait

Nausea

Numbness (in ipsilateral face and/or contralateralbody)

Nystagmus

NystagmusNystagmus

Repetitive, back-and-forth, involuntary eyemovements initiated by slow drifts awayfrom the visual target

Pendular nystagmus consists of slowsinusoidal oscillations

Jerk nystagmus is characterized by analternating slow drift and a quick correctivephase

NystagmusNystagmus

Spontaneous nystagmus may imply an acuteperipheral vestibular lesion and may occurin the symptom-free interval in patientswith vestibular migraine

Jerk nystagmus with the quick phaseindicating the unaffected side

NystagmusNystagmus

Purely vertical (upbeat or downbeat) ortorsional spontaneous nystagmus isindicative of a central vestibular lesion

Nystagmus due to a central lesion usuallycannot be suppressed with visual fixation

NystagmusNystagmus

Positional downbeat vertical or skewnystagmus: Posterior fossa lesions (Arnold-Chiari malformation or another compressivelesion at the foramen magnum)

NystagmusNystagmus

Pendular nystagmus occurs most commonlyin patients with multiple sclerosis and brainstem stroke

Cervical Artery DysfunctionCervical Artery Dysfunction

Non-ischaemic signs and symptoms

Ischaemic signs and symptoms

Vertebrobasilar system

Internal carotid artery

NonNon--Ischaemic Signs andIschaemic Signs andSymptoms VASymptoms VA

Ipsilateral posterior neck pain

Ipsilateral occipital headache

Sudden-onset and severe

Described as stabbing, pulsating, aching,“thunderclap”, sharp, or of an unusual character

“A headache unlike any ever experiencedbefore…”

Rarely C5-C6 nerve root impairment due to localneural ischaemia

Ischaemic Signs andIschaemic Signs andSymptoms VASymptoms VA

Five Ds And 3 Ns

Vomiting

Loss of short-term memory

Vagueness

Hypotonia and limb weakness affecting arm or leg

Anhydrosis: lack of facial sweating

Hearing disturbances

Horner syndrome

Ischaemic Signs andIschaemic Signs andSymptoms VASymptoms VA

Malaise

Perioral dysaesthesia

Photophobia

Clumsiness

Agitation

Cranial nerve palsies

Hindbrain stroke: Wallenberg or locked-insyndrome

NonNon--Ischaemic Signs andIschaemic Signs andSymptoms ICASymptoms ICA

Ipsilateral upper and mid-cervical pain

Ipsilateral fronto-temporal or peri-orbitalheadache

Sudden onset, severe, uncommon character

Horner syndrome

Pulsatile tinnitus

Cranial nerve palsies

NonNon--Ischaemic Signs andIschaemic Signs andSymptoms ICASymptoms ICA

Ipsilateral carotid bruit

Neck swelling

Scalp tenderness

Anhydrosis face

Ischaemic Signs andIschaemic Signs andSymptoms ICASymptoms ICA

TIA

Middle cerebral artery distribution stroke

Retinal infarction

Amaurosis fugax: Temporary blindness

Local patchy blurring of vision: Scintillatingscotomata

Weakness extra-ocular muscles

Protrusion eye

Swelling eye or conjunctiva

Horner syndrome

Carotid BruitCarotid Bruit

56% sensitivity and 91% specificity for detectionof a 70-99% carotid stenosis when compared withcolor duplex ultrasound

Implication?

Magyar MT, et al. Carotid artery auscultation: Anachronismor useful screening procedure? Neurol Res 2002;24:705-708

Cranial Nerve PalsiesCranial Nerve Palsies

Relevant to the physical examination are thecranial nerve palsies that may occur with cervicalartery dissection

Dissection of the ICA mainly causes CN IX-XIIdysfunction with the hypoglossal nerve initiallyaffected and then the other three nerves;eventually all cranial nerves except the olfactorycan be affected

Cranial nerve palsies are part of the ischaemicpresentation of a vertebral artery dissection

Cranial Nerve PalsiesCranial Nerve Palsies

Cranial nerve Test L/RI. Olfactory Identify different odors + -II. Optic Test visual fields (Confrontation method) + -III. Oculomotor Upward, downward, and medial gaze + -IV. Trochlear Downward and lateral gaze + -V. Trigeminal Corneal reflex, face sensation, clench teeth + -VI. Abducens Lateral gaze + -VII. Facial Close eyes tight, smile, whistle, puff cheeks + -VIII. Vestibulo-cochlear Hear watch ticking, hearing tests, balance tests + -IX. Glossopharyngeal Gag reflex, ability to swallow + -X. Vagus Gag reflex, ability to swallow, say “Ahhh” + -XI. Accessory Resisted shoulder shrug + -XII. Hypoglossal Tongue protrusion (Observe for deviation) + -

Horner SyndromeHorner Syndrome

Four physical signs: miosis, ptosis,enophthalmos, and anhydrosis

Miosis or inability to dilate a pupil

Paralysis of the dilatator pupillae muscle


Incomplete ptosis or droopy upper eyelid

Weakness tarsalis superior muscle

Ptosis can occur due to weakness in the levatorpalpebrae, a voluntary muscle innervated by theoculomotor nerve or as a result of weakness in thesympathetically innervated tarsalis superiormuscle

Ptosis can also occur congenitally, and it canoccur as a familial condition, with increasing age,fatigue, depression, and drowsiness


Enophthalmus or deeper-seated eye

Weakness orbitalis muscle

Anhydrosis or decreased sweating

Affects ipsilateral head and shoulders

Syndrome often incomplete

Especially the enophthalmus and the anhydrosisare frequently absent

Miosis is often only noticeable in a darkenvironment when the unaffected pupil dilates andthe affected pupil does not


Three possible locations for the lesion:

The central neuron runs from the hypothalamus tothe ciliospinal center and is located in the cervicalspinal cord (C8-T2)

This may occur as a result of ischaemic processesaffecting the medulla (i.e., vertebrobasilarischaemia) or as a result of insult to the spinal cord


The secondary neurons run from theciliospinal center by way of the nerve rootsC8-T2 to the sympathetic ganglia andthrough these ganglia to the superiorcervical or stellate ganglion

This may occur as a result of, e.g.,syringomyelia or a tumor of the apex of thelung


The tertiary neuron runs from the stellateganglion to the dilatator pupillae and thevascular supply to the iris

This may occur due to carotid ischaemia

Clinical implications?

Note: A congenital form of Horner’ssyndrome exists and can be recognized byunequal coloring of both irises

Thunderclap HeadacheThunderclap Headache

Headache: DifferentialHeadache: DifferentialDiagnosisDiagnosis

Cervicogenic headache

Tension-type headache

Migraine headache

Cervicogenic HeadacheCervicogenic Headache

Pain, referred from a source in the neck andperceived in one or more regions of the headand/or face, fulfilling criteria C and D

Clinical, laboratory and/or imaging evidence of adisorder or lesion within the cervical spine orsoft tissues of the neck known to be, or generallyaccepted as, a valid cause of headache

Cervicogenic HeadacheCervicogenic Headache

Evidence that the pain can be attributed to the neckdisorder or lesion based on at least one of thefollowing:

1. Demonstration of clinical signs that implicate asource of pain in the neck

2. Abolition of headache following diagnosticblockade of a cervical structure or its nervesupply using placebo- or other adequate controls

Pain resolves within 3 months after successfultreatment of the causative disorder or lesion

Referral Pattern UpperReferral Pattern UpperTrapezius MuscleTrapezius Muscle

Referral Pattern LevatorReferral Pattern LevatorScapulae MuscleScapulae Muscle

Referral PatternReferral PatternSternocleidomastoid MuscleSternocleidomastoid Muscle

Referral Pattern TemporalisReferral Pattern TemporalisMuscleMuscle

Referral Patterns Splenius CapitisReferral Patterns Splenius Capitis

(Left) and Cervicis (Right) Muscles(Left) and Cervicis (Right) Muscles

Referral Patterns SemispinalisReferral Patterns SemispinalisCervicis (Left) and Capitis (Right)Cervicis (Left) and Capitis (Right)

MusclesMuscles

TensionTension--Type HeadacheType Headache

Hypothesized to be related to myofascial triggerpoints

Prolonged nociceptive input may lead to centralsensitization

Amplification of receptiveness of central pain-signaling neurons to input from low-thresholdmechanoreceptors

Clinically characterized by the presence ofhyperalgesia and/or allodynia

TensionTension--Type HeadacheType Headache

Headache has at least two of the following characteristics:

1. Bilateral location

2. Pressing/tightening (non-pulsating) quality

3. Mild to moderate intensity

4. Not aggravated by routine physical activity such aswalking or climbing stairs

Both of the following:

1. No more than one of photophobia, phonophobia or mildnausea

2. Neither moderate or severe nausea nor vomiting

Not attributed to another disorder

Migraine with AuraMigraine with Aura

At least 2 attacks fulfilling criteria 2-4

Aura consisting of at least one of the following,but no motor weakness:

1. Fully reversible visual symptoms includingpositive features (e.g., flickering lights, spots orlines) and/or negative features (i.e., loss of vision)

2. Fully reversible sensory symptoms includingpositive features (i.e., pins and needles, peri-oralparaesthesiae) and/or negative features (i.e.,numbness)

3. Fully reversible dysphasic speech disturbance

Migraine with AuraMigraine with Aura

At least two of the following:

1. Homonymous visual symptoms and/orunilateral sensory symptoms

2. At least one aura symptom develops graduallyover ≥5 minutes and/or different aura symptomsoccur in succession over ≥5 minutes

3. Each symptom lasts ≥5 and ≤60 minutes

Headache fulfilling criteria Migraine without aurabegins during the aura or follows aura within 60minutes

Not attributed to another disorder

CPR Migraine HeadacheCPR Migraine HeadacheDiagnosisDiagnosis

Five questions:

1. Is it a pulsating headache

2. Does it last between 4 and 72 hourswithout medication?

3. Is it unilateral?

4. Is there nausea

5. Is the headache disabling (disrupting dailyactivities)?

CPR Migraine HeadacheCPR Migraine HeadacheDiagnosisDiagnosis

≥ 4 questions yes: LR+ 24 (95% CI: 1.5-388)

3 questions yes: LR+ 3.5 (95% CI: 1.3-9.2)

1 or 2 questions yes: LR+ 0.41 (95% CI:0.32-0.52)

Mnemonic POUNDing: Pulsating, Durationof 4-72 hours, Unilateral, Nausea, Disabling

Relevance thunderclapRelevance thunderclapheadacheheadache

In 27 cases of non-CSMT VAD this headachepreceded the neurological symptoms:

By less than 1 day in < 30% of cases

By 1-3 days in 15%

By 1-2 weeks in 30%

By > 3 weeks in 25%

Terrett AGJ. Vertebrobasilar stroke following spinal manipulation therapy. In:Murphy R. Conservative Management of Cervical Spine Syndromes (2000)

Risk ManagementRisk Management

Manipulation or mobilization

Type of manipulative technique

Upper versus lower cervical techniques

Mobilization or Manipulation?Mobilization or Manipulation?

Michaeli (1993): Questionnaire sent tomanipulative physiotherapists in SouthAfrica

228,050 procedures

Only minor adverse effects reported formanipulation

29 patients receiving cervical spinalmanipulation reported 52 complications

Mobilization or Manipulation?Mobilization or Manipulation?

However:

58 patients receiving spinal mobilization to thecervical spine reported 129 complications

One mobilization patient suffered a CVA

Implication for risk reduction?

Michaeli A. Reported occurrence and nature of complications followingmanipulative physiotherapy in South Africa. Aust J Physiother1993;39:309-315

Manipulation: Effect ofManipulation: Effect ofTechnique?Technique?

Rotation appears to place the greatest stress onarterial structures, especially in the upper cervicalspine

However, Haldeman et al (2002): review 64medicolegal reports

Strokes noted after any type of manipulation

Including rotation, extension, side bending, non-force, and neutral position manipulation

Haldeman S, et al. Stroke, cervical artery dissection, and cervical spine

manipulation therapy. J Neurol 2002;249:1098-1104

Manipulation: Effect of Level?Manipulation: Effect of Level?

Most reported site of VA damage is at C1-C2

Includes traumatic and spontaneousdissections

Mas JL, et al. Extracranial vertebral artery dissections: A review of 13 cases. Stroke1987;18:1037-1047

Mokri B, et al. Spontaneous dissections of the vertebral arteries. Neurology 1988;38:880-885

Saeed AB, et al. Vertebral artery dissection: Warning symptoms, clinical features, andprognosis in 26 patients. Can J Neurol Sci 2000;27:292-296.


Cervical manipulation definable event withevidence of a mechanical effect

Provided and recorded by third parties unlikeetiologic mechanisms such as shoulder checking,hair washing, etc.

“Not to say less recordable mechanical events areless related to dissection”

Kawchuk GN, et al. The relationship between the spatial distribution of vertebral arterycompromise and exposure to cervical manipulation. J Neurol 2008;255:371-377.


Populations studied

5-year retrospective review yielding a cohort of 25patients with VA dissection not related to majortrauma or CSMT from Foothills Hospital, Calgary,AB

26 of 64 cases reported by Haldeman et al fromretrospective case review article

Diagnostic imaging or reports had to be availableto determine location of VA dissection


V3 segment most commonly dissected

Prevalence ratio (PR) V3 versus V1prevalence in CSMT group = 8.46 (95%CI: 3.53-20.24)

PR V3 versus V1 in non-CSMT group =4.00 (95% CI: 1.43-11.15)


Note: Higher prevalence irrespective of exposureto CSMT

“Demonstrates the impact of everyday movementsand postures [on this mechanically morevulnerable segment]”

Age and gender not found to be significant factors

But: V3 vulnerability augmented by CSMTexposure


However, multiple site lesions alsosignificantly more common in both groups

CSMT: PR = 2.67 (95% CI: 1.98-3.58)

No CSMT: PR = 2.44 (95% CI: 1.81-3.29)

Interpretation?


Report of compression at C6 secondaryto osteophyte arising from superiorfacet C6

Citow JS, Macdonald RL. Posterior decompression of the vertebral arterynarrowed by cervical osteophyte: Case report. Surg Neurol1999;51:495-498.

Emergency Procedures: WhatEmergency Procedures: Whatif the Unthinkable Happens…?if the Unthinkable Happens…?Onset of symptoms indicated in 138 of 185 cases:

69%: during CSMT

3%: within minutes of CSMT

8.5%: within 1 hour of CSMT

8.5%: 1-6 hours post-CSMT

5%: 7-24 hours post-CSMT

6%: >24 hours post-CSMT

Emergency Procedures: WhatEmergency Procedures: Whatif the Unthinkable happens…?if the Unthinkable happens…? Do not re-manipulate the patient’s neck

Observe the patient: Transient signs andsymptoms or cervicogenic proprioceptivedizziness?

Refer the patient: rescue and recoveryposition, do not give the patient anything toeat or drink (dysphagia), note the time, call911

I would like to thank DeborahI would like to thank DeborahCracknell for inviting me to doCracknell for inviting me to do

this presentation for you allthis presentation for you allthis afternoon.this afternoon.

Any questions?Any questions?

cervical artery presentation

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